ArticleThe EMBO journal2017
Carcinogen susceptibility is regulated by genome architecture and predicts cancer mutagenesis.
Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 86 citations in OpenAlex.
- Non-coding DNA dynamics and its roles as a physical barrier in genome safeguarding across early development and evolution.Heredity · 2026Review
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- Interplay of replication timing, DNA repair, and translesion synthesis in UV mutagenesis in yeast.Nucleus (Austin, Tex.) · 2025Article
- Nuclear lamina-associated domain biogenesis is regulated by nuclear pore density during embryogenesis and mediates UV protection.bioRxiv : the preprint server for biology · 2025Article
- p53 Regulates Nuclear Architecture to Reduce Carcinogen Sensitivity and Mutagenic Potential.bioRxiv : the preprint server for biology · 2025Article
- Monitoring the rate and variability of somatic genomic alterations using long-read sequencing.Scientific reports · 2025Article
- Ultraviolet damage and repair maps inGenome research · 2025Article
- The epigenetic landscape shapes smoking-induced mutagenesis by modulating DNA damage susceptibility and repair efficiency.Nucleic acids research · 2025Article
- Review
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Methods and applications of genome-wide profiling of DNA damage and rare mutations.Nature reviews. Genetics · 2024Review
- Review
- Cell cycle gene alterations associate with a redistribution of mutation risk across chromosomal domains in human cancers.Nature cancer · 2024Article
- Chromosomal positioning and epigenetic architecture influence DNA methylation patterns triggered by galactic cosmic radiation.Scientific reports · 2024Article
- Sequence dependencies and mutation rates of localized mutational processes in cancer.Genome medicine · 2023Article
- Spatial mapping of the DNA adducts in cancer.DNA repair · 2023Review
- The interplay of 3D genome organization with UV-induced DNA damage and repair.The Journal of biological chemistry · 2023Article
- The 8q24 region hosts miRNAs altered in biospecimens of colorectal and bladder cancer patients.Cancer medicine · 2023Article
- Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.Cancers · 2023Review
- Circle Damage Sequencing for Whole-Genome Analysis of DNA Damage.Methods in molecular biology (Clifton, N.J.) · 2023Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The development of many sporadic cancers is directly initiated by carcinogen exposure. Carcinogens induce malignancies by creating DNA lesions (i.e., adducts) that can result in mutations if left unrepaired. Despite this knowledge, there has been remarkably little investigation into the regulation of susceptibility to acquire DNA lesions. In this study, we present the first quantitative human genome-wide map of DNA lesions induced by ultraviolet (UV) radiation, the ubiquitous carcinogen in sunlight that causes skin cancer. Remarkably, the pattern of carcinogen susceptibility across the genome of primary cells significantly reflects mutation frequency in malignant melanoma. Surprisingly, DNase-accessible euchromatin is protected from UV, while lamina-associated heterochromatin at the nuclear periphery is vulnerable. Many cancer driver genes have an intrinsic increase in carcinogen susceptibility, including the
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.